Basics & Negative feedback
- External environment changes effect the internal environment.
- Keeping your internal environment constant is vital to stop cells from malfunctioning/being damaged, and homestasis does just this.
- Especially important to maintain temperature (too high & enzymes can become denatured, too low & the enzyme activity is reduced-optimum 37'C) and pH (too high/low then enzymes are denatured- optimum is pH7)
- Glucose concentration is also an important factor to maintain. Too high- water potential reduced so H2O molecules diffuse by osmosis out of cells into blood (cells shrivel up & die) Too low- cells stop working as there's not enough glucose to provide energy.
- Receptors detect when a level is too high/low, info is sent via nervous/hormonal system to the effectors, which counteract the change.
- This is negative feedback, which brings all the levels back to normal.
- Multiple feedback systems mean a faster return to normal, as it actively increases/decreases a level e.g. in a car, take foot off accelerator slows you down, but using the brake aswell would slow you down a lot faster.
- Amplifies any change to levels.
- Positive feedback makes the levels which have changed fluctuate further away from the norm.
- Useful to quickly activate something e.g. blood clot
- Not involved in homeostasis as it doesn't keep environment constant.
- Low body temperature (below 35'C)
- Result of heat being lost from the body faster than it's being produced.
- Brain stops working properly, shivering stops making body even colder.
- Positive feedback makes body temperature drop even further (going away from the norm temperature) unless help is found.
Control of body temperature
Ectotherms (e.g. reptiles/fish):
- Can't control temperature internally, change behaviour instead-go in sun etc
- Internal temperature depends on their external surroundings.
- More active at higher temperatures & less active at low temperatures.
- Variable metabolic rate, don't generate a lot of heat themselves.
Endotherms (e.g. mammals/birds):
- Control body temperature internally & by behaviour (by finding shade etc).
- Internal temperature less affected by external temperature (up to a point).
- Can be active at any external temperature (up to a point).
- high metabolic rate & generate a lot of heat from metabolic reactions.
Mammalian methods of controlling body temperature
- Sweating- secreted from sweat glands, then evaporates, cooling skin.
- Hairs lie flat- erector pili muscles relax, less air is trapped- more heat lost.
- Vasodilation- arterioles near surface dilate and more blood flows through capillaries, so more heat is lost by radiation.
- Shivering- muscles contract in spasms, more heat is produced (increased rate of respiration).
- Hormones- adreneline released- increases metabolic rate- more heat.
- Less sweat- reduced amount of heat loss.
- Hairs stand up-erector pili muscles contract, hairs trap air& insulate body.
- Vasoconstriction- arterioles constrict, less blood flows, reduces heat loss.
Hypothalamus' role in controlling body temperature
- Part of the brain (the hypothalmus) maintains a constant body temperature.
- Gets info about both internal & external temperature from thermoreceptors.
- Internal temperature info is from thermoreceptors in hypothalmus which detect blood temperature.
- External temperature info is from thermoreceptors in skin which detect skin temperature.
- Thermoreceptors send impulses along sensory neurones to hypothalmus, which sends impulses along motor neurones to effectors (muscles/glands).
- All unconcious- via the autonomic nervous system.
- Effectors use methods shown on the previous card ("mammalian methods...") to return temperature to normal (i.e. 37'C).
Controlling blood glucose concentration
- Cells in pancreas monitor blood glucose concentration (BGC)
- BGC rises after eating carbohydrates (get energy from these) and falls after exercise (more glucose is used in respiration to produce energy).
- Controlled by the hormones insulin & glucagon (negative feedback)
- Beta cells secrete insulin & alpha cells secrete glucagon.
Insulin Lowers BGC when it's too high...
- Binds to receptors in liver & muscle cells and increases the permeability to glucose, so cells take up more glucose.
- Also activates enzymes which convert glucose into glycogen (glycogenesis).
- Increases rate of respiration of glucose, esp. in muscle cells.
Glucagon raises BGC when it's too low...
- Binds to specific receptors in liver cells, activates enzymes which convert glycogen into glucose (glycogenolysis) and also converts amino acids into glucose (gluconeogenesis)
- Glucagon decreases rate of respiration of glucose in cells.
- Hormone which is secreted from adrenal glands (above your kidneys) when there's a low blood glucose concentration (BCG)
- Binds to receptors in liver cell membranes
- Activates glycogenolysis (glycogen --> glucose)
- Inhibits glycogenesis (glucose --> glycogen)
- Inhibits insulin secretion & activates glucagon secretion.
- Body is ready for action as it has more glucose available for muscles to use in respiration.
Can also activate glycogenolysis inside a cell...
- Adrenaline& glucagon bind to receptors- activate adenylate cyclase enzyme.
- Enzyme converts ATP into a chemical messenger ("second messenger").
- Second messenger called cyclic AMP (cAMP).
- cAMP activates chain of reactions: glycogen --> glucose (glycogenolysis)
Diabetes is when blood glucose concentration can't be controlled properly...
- Beta cells (in islets of langerhans) don't produce any insulin
- After eating, BGC levels rise&stay high-hyperglycaemia- can end in death.
- Kidneys can't reabsorb extra glucose, so some of it is excreted in urine.
- Injections help treat this, but too many and hypoglycaemia can occur (dramatic drop in BGC levels). Eating regularly & less sugar also helps.
- Usually aquired later in life- linked to obesity.
- Beta cells don't produce enough insulin/ body cells dont respond properly to insulin (e.g. their insulin receptors on membranes don't work.)
- Results in cells not taking up enough glucose, so BGC levels are high.
- Treated by losing weight and controlling amount of sugars eaten.
- Follicle develops in the ovary.
- Ovulation- egg is released.
- Uterus lining thickens so fertilised egg can implant.
- Corpus luteum (corp lut.) develops from follicle remains.
- No fertilisation- lining breaks down & leaves body (menstruation).
- Follicle-stimulating hormone (FSH)- stimulates follicle to develop.
- Luteinising hormone (LH)- stimulates ovulation & development of corp lut.
- Oestrogen (O)- stimulates thickening of uterus
- Progesterone (P)- maintains thick uterus lining
- FSH & LH secreted by anterior pituitary gland. O & P secreted by ovaries.
Menstrual Cycle 2
- High FHS- follicle develops- releases O. FSH stimulates ovaries to release O
- O conc. rises- stimulates lining to thicken. Inhibits FSH being released.
- O conc. peaks- stimulates pituitary gland to release LH and FSH.
- Surge of LH- stimulates ovulation. Corp lut. develops & releases P.
- P conc. rises- inhibits FSH & LH release. Lining maintained. No fertilisation- corp lut. breaks down & stops releasing P.
- P conc. falls- FSH & LH conc. increase (no longer inhibited by P). Lining isn't maintained, so it breaks down & leaves body (menstruation).
- FSH stimulates release of O. O inhibits release of FSH.- no more follicles!
- LH stimulates corp. lut to develop producing P, P inhibits release of LH- no more follicles develop & lining broken down if no fertilisation occurs.
- O stimulates release of LH, which stimulates release of more O etc etc.